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. Author manuscript; available in PMC: 2014 Feb 7.
Published in final edited form as: Mol Cell. 2013 Feb 7;49(3):379–387. doi: 10.1016/j.molcel.2013.01.019

Figure 1.

Figure 1

Nutrient sensing and metabolism pathways. AMP-activated kinase (AMPK) is activated by energy stress and promotes catabolic pathways to produce ATP while switching off ATP-consuming anabolic pathways. In contrast, mammalian target of rapamycin complex 1 (mTORC1) activation under nutrient-sufficiency leads to significant elevation of anabolic processes, such as protein and lipid synthesis. Abbreviations are: GLU4, glucose transporter type 4; CPT1, Carnitine Palmitoyltransferase-1; TAK1, TGFβ-activated kinase 1; LKB1, liver kinase B1 (a key AMPK activator tumor suppressor); CAMKKβ, Calmodulin-dependent protein kinase kinase β; ACC, acetyl CoA carboxylase; PFK2, Phosphofructokinase 2; GS, glycogen synthase; HDACs, histone deacetylases; CRTC2, CREB-regulated transcription co-activator 2; FOXO, forkhead box protein O; CREB, cAMP response element-binding protein; ULK, UNC-51-like kinase; FIP200, 200 kDa FAK family kinase-interacting protein; ATG, autophagy-related; PI3K, phosphoinositide 3-kinase; IRS1, insulin receptor substrate 1; PTEN, phosphatase and tensin homologue; PDK1, 3-phosphoinositide-dependent protein kinase 1; TSC1/2, tuberous sclerosis 1/2; Rheb, Ras homologue enriched in brain; v-ATPase, vacuolar H+-adenosine triphosphatase; 4E-BP1, eukaryotic initiation factor 4E-binding protein 1; S6K, ribosomal S6 kinase; Ragulator, a protein complex responsible for lysosomal recruitment and activation of Rag GTPases; PGC1α, peroxisome proliferator-activated receptor-γ coactivator 1α; PPARγ, peroxisome proliferator-activated receptor-γ; SREBP, sterol regulatory element-binding protein; HIF, Hypoxia-inducible factors. Stimulatory interactions are indicated with ↓ and inhibitory interactions are indicated with ⊥.